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T Mitsuma

Publications and source records attributed to T Mitsuma.

At least 361 records · Page 20Linked to original sources
PubMed1975

[Studies of various factors in thyrotropoin releasing hromone TRH) radioimmunoassay for serum (author's transl)].

To study the significance of TRH in the hypothalamo-pituitary-thyroid axis measurement of TRH in body fluid are needed. We previously reported TRH radioimmunoassay for urine. TRH radioimmunoassay for serum has not established yet, because TRH immunoreactivity is inactivated with serum. We investigated effects of various factors on this inactivation and method for prevention of this inactivation. Synthetic TRH was added to normal human serum at 4 degrees C and incubated at 60 degrees C, 37 degrees C, 20 degrees C, 4 degrees C or -20 degrees C for various intervals. After incubation, recovery of TRH was measured. After one hour incubation, recovery of TRH was 9.2% at 37 degrees C, 34.5% at 20 degrees C, 100% at 4 degrees C or -20 degrees C. Incubation of TRH serum mixtures at 65 degrees C after incubation at 37 degrees C resulted in some recovery of TRH. After one hour incubation at 37 degrees C, recovery of TRH was 9.2% at serum pH 7.0, 100% at serum pH 3.0 to 5.0 or 11.0. Recovery of TRH was increased in accordance with stepwisely increase of serum dilution. Concentrations of serum thyroid hormone did not affect recovery of TRH. Smaller quantities of TRH were more rapidly inactivated. Inactivation of TRH immunoreactivity could be prevented addition of BAL (over 0.25 mg/ml) or mixture of 8-Hydroxyquinoline (HQ) and Tween 20(T) (over 0.1 mg/ml of HQ and 1 lmg/ml of T). Duration of effectiveness of BAL was short. Effectiveness of HQT continued for 12 weeks, if HQT treated serum was stored at -20 degrees C. From above data it was suggested that TRH immunoreactivity might be inactivated with enzyme system and other factors and TRH levels in the serum might be able to measure with addition of HQT to serum.

Chelating Agents↗
PubMed1975

In vitro reconstitution of anti-sheep erythrocyte antibody response of T cell-depleted spleen cells by allogeneic T cells or by factors derived from them.

Restoration of the impaired antibody response to sheep erythrocytes (SRBC) in cultures of mouse spleen cells, which were deprived of thymus-derived lymphocytes (T cells) by treatment with anti-mouse brain-associated theta (BA theta) antiserum and complement, was studied by adding a small portion of syngeneic or allogeneic normal spleen cells in vitro. Allogeneic spleen cells had a far greater effect than syngeneic spleen cells on the restoration, as far as the normal spleen cells added were able to recognize the alloantigens on the anti-BA theta serum-treated spleen cells (bone marrow-derived lymphocytes). Treatment of the allogeneic spleen cells with mitomycin C did not affect their activity in the restoration of the impaired antibody response. The possibility that the role of T cells in the antibody response to SRBC may be replaced by a nonspecific mediator derived from T cells reacting with allogeneic cells was proven by the finding that supernatant of the mixed allogeneic spleen cell cultures restored the impaired anti-SRBC antibody response of the T cell-depleted spleen cells. The effect of such culture supernatant on the restoration of the antibody response was greatest when it was added to the T cell-depleted spleen cell cultures one day after cultivation with SRBC, suggesting that the effectiveness may result from triggering of the proliferation and differentiation of antibody-forming cell precursors, which have already reacted with the antigen, to antibody-forming cells.

Animals↗
PubMed1973

Modulation of pituitary responsiveness to thyrotropin-releasing hormone by triiodothyronine.

The relative roles of triiodothyronine (T(3)) and thyroxine (T(4)) in modulating pituitary responsiveness to thyrotropin-releasing hormone (TRH) have been assessed. (a) 10 hyperthyroid patients with elevated serum T(2) and T(4) levels showed no pituitary response to TRH. After 2 wk of propylthiouracil therapy T(4) levels had fallen to normal in only five patients while T(2) levels were normal in all. Pituitary responsiveness to TRH returned in all patients with normal or high T(4) concentrations. (b) Patients with isolated elevations of serum T(3) (T(3) toxicosis) failed to respond to TRH. TRH responsiveness was restored when T(3) levels fell to normal after propylthiouracil therapy. (c) When pituitary responsiveness to TRH was tested 60 min after a single oral dose of 50 mug of T(3), which increased serum T(3) levels to slightly above the normal range, no rise in thyrotropin (TSH) was seen in six subjects. These findings indicate that T(3) elevations alone can rapidly inhibit pituitary responsiveness to TRH.

Administration, Oral↗